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Harakiri, BCL2 interacting protein

DP5, Hrk, Bcl-2-interacting protein, Harakiri
Activator of apoptosis Hrk regulates apoptosis through interaction with death-repressor proteins Bcl-2 and Bcl-X(L). The HRK protein lacks significant homology to other BCL2 family members except for an 8-amino acid region that was similar to the BCL2 homology domain-3 (BH3) motif of BIK. HRK interacts with BCL2 and BCLXL via the BH3 domain, but not with the death-promoting BCL2-related proteins BAX, BAK, or BCLXS. HRK localizes to membranes of intracellular organelles in a pattern similar to that previously reported for BCL2 and BCLXL. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: bcl-2, CAN, Bax, PrP, ACID
Papers on DP5
Ikaros, Helios, and Aiolos protein levels increase in human thymocytes after β selection.
Yankee et al., Kansas City, United States. In Immunol Res, Jan 2016
In each group of patients, CD3(-) ISP and DP thymocytes were subdivided into ISP1, ISP2, DP1, DP2, DP3, DP4, and DP5 developmental stages according to their expression of CD28, CD44, CD1a, CD7, CD45RO, and CD38.
Bis Expression in Patients with Surgically Resected Lung Cancer and its Clinical Significance.
Lee et al., Seoul, South Korea. In Ann Surg Oncol, Dec 2015
BACKGROUND: Bis, also known as BAG3, has been identified as a Bcl-2-interacting protein that enhances cellular anti-apoptotic activity.
FOXO1 activation is an effector of SYK and AKT inhibition in tonic BCR signal-dependent diffuse large B-cell lymphomas.
Juszczynski et al., Warsaw, Poland. In Blood, Dec 2015
Since HRK is the key effector of SYK inhibition, we characterized a mechanism linking FOXO1 activation and HRK induction that involves caspase-dependent cleavage of HRK's transcriptional repressor DREAM.
In vitro digestion and fermentation properties of linear sugar-beet arabinan and its oligosaccharides.
Han et al., Ch'ŏngju, South Korea. In Carbohydr Polym, Nov 2015
DP4 (20.1%), and DP5 (1.16%).
Bid chimeras indicate that most BH3-only proteins can directly activate Bak and Bax, and show no preference for Bak versus Bax.
Kluck et al., Australia. In Cell Death Dis, 2014
To generate each BH3-only protein as a recombinant protein that could efficiently target mitochondria, we developed recombinant Bid chimeras in which the BH3 domain was replaced with that of other BH3-only proteins (Bim, Puma, Noxa, Bad, Bmf, Bik and Hrk).
Complete genome sequence of and proposal of Thermofilum uzonense sp. nov. a novel hyperthermophilic crenarchaeon and emended description of the genus Thermofilum.
Kublanov et al., Kaliningrad, Russia. In Stand Genomic Sci, 2014
The average nucleotide identities between genome of strain 1807-2 and T. pendens strain HRK 5(T) and "T.
Extracellular Polyhydroxyalkanoate Depolymerase by Acidovorax sp. DP5.
Amirul et al., George Town, Malaysia. In Enzyme Res, 2014
Among the isolates, DP5 exhibited the largest clearing zone with a degradation index of 6.0.
SYK inhibition modulates distinct PI3K/AKT- dependent survival pathways and cholesterol biosynthesis in diffuse large B cell lymphomas.
Shipp et al., Boston, United States. In Cancer Cell, 2013
Herein, we characterize distinct SYK/PI3K-dependent survival pathways in DLBCLs with high or low baseline NF-κB activity including selective repression of the pro-apoptotic HRK protein in NF-κB-low tumors.
Deficiency of pro-apoptotic Hrk attenuates programmed cell death in the developing murine nervous system but does not affect Bcl-x deficiency-induced neuron apoptosis.
Roth et al., Birmingham, United States. In J Histochem Cytochem, 2011
Hrk deficiency does not significantly attenuate the widespread apoptosis seen in the Bcl-x (-/-) embryonic nervous system, indicating that other BH3-only molecules, alone or in combination, may regulate BAX activation in immature neurons.
Intrinsic order and disorder in the bcl-2 member harakiri: insights into its proapoptotic activity.
de Alba et al., Madrid, Spain. In Plos One, 2010
These results are used to propose a tentative structural model of how Harakiri works.
Clinical effectiveness and cost-effectiveness of stem cell transplantation in the management of acute leukaemia: a systematic review.
Chen et al., Birmingham, United Kingdom. In Health Technol Assess, 2010
Included randomised controlled trials (RCTs) and donor versus no donor (DvND) studies were mapped to the evidence covered in existing systematic reviews and meta-analyses according to a framework of 12 decision problems (DPs): DP1 related to SCT in adults with AML in first complete remission (CR1); DP2 to adults with AML in second or subsequent remission or with refractory disease (CR2+); DP3 to children with AML in CR1; DP4 to children with AML in CR2+; DP5 to adults with ALL in CR1; DP6 to adults with ALL in CR2+; DP7 to children with ALL in CR1; DP8 to children with ALL in CR2+; DP9 to comparison of different sources of stem cells in transplantation; DP10 to different conditioning regimens; DP11 to the use of purging in autologous SCT; and DP12 to the use of T-cell depletion in allogeneic SCT.
Characterization of a novel interaction between Bcl-2 members Diva and Harakiri.
de Alba et al., Madrid, Spain. In Plos One, 2009
analysis of a novel interaction between Bcl-2 members Diva and Harakiri
Signaling by IL-1beta+IFN-gamma and ER stress converge on DP5/Hrk activation: a novel mechanism for pancreatic beta-cell apoptosis.
Eizirik et al., Brussels, Belgium. In Cell Death Differ, 2009
The inactivation of hrk protein protects -cells from IL-1beta+IFN-gamma and chemical Endoplasmic Reticulum stress-mediated cell death.
The role of HRK gene in human cancer.
Konishi et al., Nara, Japan. In Oncogene, 2008
Aberrant 5'-CpG methylation status and loss of heterozygosity on 12q13.1 are associated with HRK expression in human malignancies, including prostate cancers, astrocytic tumors and primary central nervous system lymphomas. Review.
Hierarchical regulation of mitochondrion-dependent apoptosis by BCL-2 subfamilies.
Cheng et al., Saint Louis, United States. In Nat Cell Biol, 2006
Extensive mutagenesis of BAX-BAK indicates that their activity is not kept in check by BCL-2-BCL-X(L)-MCL-1. Anti-apoptotic BCL-2 members are differentially inactivated by the remaining 'inactivator' BH3-only molecules including BAD, NOXA, BMF, BIK/BLK and HRK/DP5.
Bcl-2 inhibition of autophagy: a new route to cancer?
Levine et al., Dallas, United States. In Cancer Res, 2006
Beclin 1, the first identified mammalian autophagy gene product, is a haploinsufficient tumor suppressor that was originally isolated as a Bcl-2-interacting protein.
Life in the balance: how BH3-only proteins induce apoptosis.
Adams et al., Australia. In Curr Opin Cell Biol, 2005
BH3-only members of the Bcl-2 intracellular protein family, which include Bim, Bmf, Bik, Bad, Bid, Puma, Noxa and Hrk, mediate many developmentally programmed and induced cytotoxic signals.
[DREAM/Calsenilin/KChIP3: a new multifunctional protein in nervous system].
Wang et al., Beijing, China. In Sheng Li Ke Xue Jin Zhan, 2005
A newly found transcription factor-DREAM can bind specifically with downstream regulatory element of genes, such as PPD, Hrk and c-Fos, and repress gene expression.
The C. elegans protein EGL-1 is required for programmed cell death and interacts with the Bcl-2-like protein CED-9.
Horvitz et al., Cambridge, United States. In Cell, 1998
The EGL-1 protein contains a nine amino acid region similar to the Bcl-2 homology region 3 (BH3) domain but does not contain a BH1, BH2, or BH4 domain, suggesting that EGL-1 may be a member of a family of cell death activators that includes the mammalian proteins Bik, Bid, Harakiri, and Bad.
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